WordNet
- of or relating to glomeruli
PrepTutorEJDIC
- 腎臓の
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- 1. 腎臓の同種移植片機能不全の鑑別診断 differential diagnosis of renal allograft dysfunction
- 2. 腎発育不全 renal hypoplasia
- 3. Chapter 2D：GFRと腎血漿流量の調節 chapter 2d regulation of gfr and renal plasma flow
- 4. 腎生検の適応および合併症 indications for and complications of renal biopsy
- 5. サルコイドーシスにおける腎疾患 renal disease in sarcoidosis
English Journal
- Valsartan slows the progression of diabetic nephropathy in db/db mice via a reduction in podocyte injury, and renal oxidative stress and inflammation.
- Zhou G, Cheung AK, Liu X1, Huang Y1.Author information 1†Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT 84108, U.S.A.AbstractHigher doses of AngII (angiotensin II) blockers are intended to optimize albuminuria reduction rather than for blood pressure control in chronic kidney disease. However, the long-term renoprotection of high-dose AngII blockers has yet to be defined. The present study sought to determine whether doses of ARB (AngII receptor blocker) that maximally reduce proteinuria could slow the progression of glomerulosclerosis in the uninephrectomized db/db mouse, a model of Type 2 diabetes. Untreated uninephrectomized db/db mice had normal blood pressure, but developed progressive albuminuria and mesangial matrix expansion between 18 and 22 weeks of age, which was associated with increased renal expression of TGFβ1 (transforming growth factor β1), PAI-1 (plasminogen-activator inhibitor-1), type IV collagen and FN (fibronectin). Treatment with valsartan in the drinking water of db/db mice from 18 to 22 weeks of age, at a dose that was determined previously to maximally reduce proteinuria, prevented the increases in albuminuria and the markers of renal fibrosis seen in untreated db/db mice. In addition, WT-1 (Wilms tumour protein-1)-immunopositive podocyte numbers were found to be lower in the untreated glomeruli of mice with diabetes. The expression of podocin and nephrin were continually decreased in mice with diabetes between 18 and 22 weeks of age. These changes are indicative of podocyte injury and the administration of valsartan ameliorated them substantially. Renal expression of TNFα (tumour necrosis factor α), MCP-1 (monocyte chemoattractant protein-1), Nox2 (NADPH oxidase 2), p22phox and p47phox and urine TBARS (thiobarbituric acid-reacting substance) levels, the markers of renal inflammation and oxidative stress, were increased during disease progression in mice with diabetes. Valsartan treatment was shown to reduce these markers. Thus high doses of valsartan not only reduce albuminuria maximally, but also halt the progression of the glomerulosclerosis resulting from Type 2 diabetes via a reduction in podocyte injury and renal oxidative stress and inflammation.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 May 1;126(10):707-20. doi: 10.1042/CS20130223.
- Higher doses of AngII (angiotensin II) blockers are intended to optimize albuminuria reduction rather than for blood pressure control in chronic kidney disease. However, the long-term renoprotection of high-dose AngII blockers has yet to be defined. The present study sought to determine whether dose
- PMID 24195695
- Fate and plasticity of renin precursors in development and disease.
- Gomez RA1, Belyea B, Medrano S, Pentz ES, Sequeira-Lopez ML.Author information 1Department of Pediatrics, University of Virginia School of Medicine, 409 Lane Road, Room 2001, Charlottesville, VA, 22908, USA, rg@virginia.edu.AbstractRenin-expressing cells appear early in the embryo and are distributed broadly throughout the body as organogenesis ensues. Their appearance in the metanephric kidney is a relatively late event in comparison with other organs such as the fetal adrenal gland. The functions of renin cells in extra renal tissues remain to be investigated. In the kidney, they participate locally in the assembly and branching of the renal arterial tree and later in the endocrine control of blood pressure and fluid-electrolyte homeostasis. Interestingly, this endocrine function is accomplished by the remarkable plasticity of renin cell descendants along the kidney arterioles and glomeruli which are capable of reacquiring the renin phenotype in response to physiological demands, increasing circulating renin and maintaining homeostasis. Given that renin cells are sensors of the status of the extracellular fluid and perfusion pressure, several signaling mechanisms (β-adrenergic receptors, Notch pathway, gap junctions and the renal baroreceptor) must be coordinated to ensure the maintenance of renin phenotype-and ultimately the availability of renin-during basal conditions and in response to homeostatic threats. Notably, key transcriptional (Creb/CBP/p300, RBP-J) and posttranscriptional (miR-330, miR125b-5p) effectors of those signaling pathways are prominent in the regulation of renin cell identity. The next challenge, it seems, would be to understand how those factors coordinate their efforts to control the endocrine and contractile phenotypes of the myoepithelioid granulated renin-expressing cell.
- Pediatric nephrology (Berlin, Germany).Pediatr Nephrol.2014 Apr;29(4):721-6. doi: 10.1007/s00467-013-2688-0. Epub 2013 Dec 15.
- Renin-expressing cells appear early in the embryo and are distributed broadly throughout the body as organogenesis ensues. Their appearance in the metanephric kidney is a relatively late event in comparison with other organs such as the fetal adrenal gland. The functions of renin cells in extra rena
- PMID 24337407
- BMP signaling and its modifiers in kidney development.
- Nishinakamura R1, Sakaguchi M.Author information 1Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, 860-0811, Japan, ryuichi@kumamoto-u.ac.jp.AbstractThe kidney develops through mutual interactions between the metanephric mesenchyme and the ureteric bud, the former of which contains nephron progenitors that give rise to glomeruli and renal tubules. Bone morphogenetic protein (BMP) signaling and its modifiers play important roles in many steps of kidney development. BMP4 inhibits ureteric bud attraction, and the BMP antagonist Gremlin is essential for the initial stage of ureteric budding. During mid-gestation, BMP7 maintains the nephron progenitors and, at the same time, sensitizes them to the ureteric bud-derived differentiation signal. Crossveinless2 is a pro-BMP factor, and its absence leads to kidney hypoplasia. After birth, when nephron progenitors have disappeared, Dullard, a phosphatase that inactivates BMP receptors, keeps BMP signaling at an appropriate level. Deletion of Dullard results in excessive BMP signaling and apoptosis of the postnatal nephrons. In this review I discuss the similarities and differences of BMP functions in kidney development, as well as in diseases.
- Pediatric nephrology (Berlin, Germany).Pediatr Nephrol.2014 Apr;29(4):681-6. doi: 10.1007/s00467-013-2671-9. Epub 2013 Nov 12.
- The kidney develops through mutual interactions between the metanephric mesenchyme and the ureteric bud, the former of which contains nephron progenitors that give rise to glomeruli and renal tubules. Bone morphogenetic protein (BMP) signaling and its modifiers play important roles in many steps of
- PMID 24217785
Japanese Journal
- Renal thrombotic microangiopathies/thrombotic thrombocytopenic purpura in a patient with primary Sjögren's syndrome complicated with IgM monoclonal gammopathy of undetermined significance.
- Koga Tomohiro,Yamasaki Satoshi,Nakamura Hideki,Kawakami Atsushi,Furusu Akira,Taguchi Takashi,Eguchi Katsumi
- Rheumatology international 33(1), 227-230, 2013
- … We experienced a case of a 61-year-old woman with primary Sjögren's syndrome (pSS) complicated with severe renal TMA/TTP following IgM monoclonal gammopathy of undetermined significance (MGUS). … She was admitted to our hospital for further evaluation of hypergammaglobulinema, acute renal failure, and severe thrombocytopenia. … Histological examination of her kidney revealed fibrin thrombi in the glomeruli and arterioles, a finding that is consistent with TMA/TTP. …
- NAID 120002383501
- A case of minimal change nephrotic syndrome with immunoglobulin A nephropathy transitioned to focal segmental glomerulosclerosis
- Hirose Misaki,Nishino Tomoya,Uramatsu Tadashi,Obata Yoko,Kitamura Mineaki,Kawazu Tayo,Miyazaki Masanobu,Taguchi Takashi,Kohno Shigeru
- Clinical and Experimental Nephrology 16(3), 473-479, 2012
- … The results of a renal biopsy indicated slight mesangial proliferation in the glomeruli by light microscopy, and an immunofluorescence study confirmed the deposition of immunoglobulin (Ig) A and C3 in the mesangial area. … A second relapse in May 2001, showed steroid resistance with renal insufficiency, and an increase in the selectivity index to 0.195. …
- NAID 80022574804
- A case of nephrotic syndrome showing collaptic glomeruli and tubulointerstitial changes
- 江口 広宣,秋草 文四郎,平本 龍吾,松本 真輔
- 日本小児腎臓病学会雑誌 25(2), 2012
- … We experienced a 10-year-old boy with steroid-resistant nephrotic syndrome accompanied with collaptic glomeruli and tubulointerstitial change such as tubules filled with urinary casts, interstitial fibrosis and inflammatory cells in interstitium. … The second renal biopsy was performed one year after combination therapy including cyclosporine treatment, which revealed no remarkable findings. …
- NAID 130003346844
Related Links
- Where Are Glomeruli Located In The Renal? What Is Glomeruli? What Is Degenerative Inflammation Of The Glomeruli? American Heritage Medical Dictionary glomerulus glo·mer·u·lus (glō-měr'yə-ləs) n. pl. glo·mer·u·li (-lī') A small ...
- the 67-kDa NPR-C-like protein is reduced by GTPγS, suggesting that this receptor is associated with a G protein in renal glomeruli. The enhanced inhibitory role of natriuretic peptides on cAMP synthesis induced by water ...
Related Pictures
★リンクテーブル★
| リンク元 | 「glomerular」「腎糸球体」「kidney glomerulus」 |
| 関連記事 | 「renal」 |
「glomerular」
- adj.
- 糸球体の、腎糸球体の
「腎糸球体」
「kidney glomerulus」
「renal」
- adj.
- 腎臓の、腎性の、腎の